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Correction for “Phylogenetic Structure in Tropical Hummingbird Correction for “Acute in Vivo Exposure to Interferon-Γ Enables Communities,” by Catherine H COLLOQUIUM PAPER NEUROSCIENCE Correction for “Phylogenetic structure in tropical hummingbird Correction for “Acute in vivo exposure to interferon-γ enables communities,” by Catherine H. Graham, Juan L. Parra, Carsten resident brain dendritic cells to become effective antigen present- Rahbek, and Jimmy A. McGuire, which appeared in Biogeo- ing cells,” by Andres Gottfried-Blackmore, Ulrike W. Kaunzner, graphy, Changing Climates, and Niche Evolution Sackler Collo- Juliana Idoyaga, Judit C. Felger, Bruce S. McEwen, and Karen quium, supplement 2, November 17, 2009, of Proc Natl Acad Sci Bulloch, which appeared in issue 49, December 8, 2009, of Proc USA (106:19673–19678; first published September 18, 2009; 10. Natl Acad Sci USA (106:20918–20923; first published November 1073/pnas.0901649106). 11, 2009; 10.1073/PNAS.0911509106). The authors note that the data discussed in this publication The authors note that the author name Judit C. Felger should have been deposited in the GenBank database, www.ncbi.nlm. have appeared as Jennifer C. Felger. The online version has been nih.gov/GenBank (accession nos. GU166869–GU167199). corrected. The corrected author line appears below. www.pnas.org/cgi/doi10.1073/pnas.0912879107 Andres Gottfried-Blackmore, Ulrike W. Kaunzner, Juliana Idoyaga, Jennifer C. Felger, Bruce S. McEwen, and Karen Bulloch COMMENTARY Correction for “Fat location defines sensation,” by Uhtaek Oh www.pnas.org/cgi/doi10.1073/pnas.0913488107 and John N. Wood, which appeared in issue 44, November 3, 2009, of Proc Natl Acad Sci USA (106:18435–18436; first published October 28, 2009; 10.1073/PNAS.0910766106). The authors note that, on page 18436, reference 1 was incorrectly listed as “in press.” This work is in fact an unpublished observation. www.pnas.org/cgi/doi10.1073/pnas.0913327107 514 | www.pnas.org Downloaded by guest on September 23, 2021 COMMENTARY Fat location defines sensation Uhtaek Oha and John N. Wooda,b,1 aWorld Class University Programme, Department of Molecular Medicine and Biopharmaceutical Chemistry, Seoul National University, Seoul 151-742, Korea; and bWolfson Institute for Biomedical Research, University College London, London WC1E 6BT, United Kingdom rachidonic acid metabolites of TRPV1 by low pH, characteristic of of allodynia has often been associated have long been known to po- damaged tissue (8), its demonstrated with events in the dorsal horn (14). In- tentiate inflammation and sen- importance in inflammatory hyperalge- triguingly, many peptide mediators asso- sitize sensory neurons. Now sia (5), and the evidence presented here ciated with small-diameter sensory neu- Alinoleic acid, an essential ␻-6 fatty acid of an important role for presynaptic rons [calcitonin gene-related peptide precursor of arachidonic acid and a ma- TRPV1 in thermal and mechanical sen- (CGRP), substance P, brain-derived jor membrane constituent of mammalian sitization (2) support a role for TRPV1 neurotrophic factor (BDNF)] have been cells, has been found to have a related as an inflammatory amplifier. It is also shown to evoke allodynia when applied role. Hargreaves and colleagues (1) have possible that TRPV1 in CNS locations intrathecally (15–17). Thus a major af- shown that oxidized linoleic acid prod- that are not involved in pain perception ferent barrage from peptidergic nocicep- ucts produced from heated skin are po- may also regulate synaptic signaling. tive neurons is likely to sensitize dorsal tent activators of TRPV1, the capsaicin Suprathreshold noxious temperatures, horn neurons that are normally wired receptor, which plays a major role in linoleic acid metabolites, and capsaicin for mechanosensitive input through the thermal hyperalgesia. They make a in the periphery activate TRPV1 to (extrasynaptic?) actions of these media- strong case that these mediators contrib- evoke heat pain. The voltage-dependent tors. Killing the dorsal horn neurons ute substantially to heat-activated mechanism of TRP activation that un- that express NK1 receptors suppresses TRPV1 currents in sensory neurons. In derlies this form of heat sensing has allodynia, and deleting the gene for this issue of PNAS, Patwardhan et al. been described by Nilius and colleagues BDNF in Nav1.8ϩ neurons also inhibits (2) extend the group’s findings to show (9), and other TRPVs have been investi- central sensitization (18, 19). Specific that depolarized spinal cord neurons gated as potential heat sensors (8). At antagonists of TRPV1 can block me- also release the same oxidized linoleic the moment, however, the molecular chanical allodynia, suggesting that pre- acid metabolites that act on TRPV1. identity of the threshold acute noxious synaptic TRPV1 activation is an impor- This release causes not only thermal heat sensor that may also be sensitized tant element in the release of pro- hyperalgesia but also mechanical allo- by pro-inflammatory lipids remains un- allodynic mediators (20). Thus afferent dynia (pain associated with a normally known, as do the set of sensory neurons barrage leading to second-order neural nonnoxious mechanical stimulus). Thus that first respond to tissue-damaging depolarization may cause the release of the same chemical mediators [9- and heat. 13-hydroxyoctadecanoic acid (9-HODE 9-HODE that amplifies the release of and 13-HODE) and related molecules] Lipid Activators of TRPV1 neuromodulators in the dorsal horn. In acting through the same receptor, A range of fats activate TRPV1, includ- this way, despite the known mechanoin- TRPV1, appear to have distinct effects ing anandamide, diacylglycerol and li- sensitivity of TRPV1, presynaptic ampli- on sensation when released either pe- poxygenase metabolites of arachidonic fication of nociceptive input through this ripherally or centrally. How can we ex- acid, the unsaturated long-chain receptor contributes to allodynia. High- plain these fascinating observations? N-acylethanolamines, and unsaturated dose peripheral capsaicin, which causes long-chain N-acyldopamines (10). Inter- a sustained depolarization of peptidergic Heat Sensing estingly, lipid activators have been asso- neurons, can cause allodynia, consistent The molecular cloning of the heat-acti- ciated with G-protein-coupled receptor with the present model (21). Pain re- vated capsaicin receptor TRPV1 by Ca- (GPCR) systems, some of which are ap- search (with drugs in mind) has focused terina, Julius, and their colleagues (3) parently analgesic—e.g., CB1 and 2 re- on mediators, rather than neuronal provided a satisfying explanation for the ceptors activated by anandamide (11). pathways, and we have limited insight hot sensation evoked by chili peppers This association makes unraveling the into the innervation of dorsal horn neu- and a potential identity for the heat- physiological actions of lipid metabolites rons above a simple lamina specificity. sensitive channels originally described by in pain pathways problematic. Interest- Given the importance of presynaptic Cesare and McNaughton (4). As soon as ingly, there is an association between TRPV1 within the dorsal horn in central the TRPV1-knockout mouse was gener- linoleic acid release and inflammation, sensitization, it will be fascinating to see ated, however, it became clear that raising the possibility that the neutraliz- which dorsal horn neurons are inner- there must be other heat sensors in sen- ing antibodies described by Patwardhan vated by these TRPV1ϩ terminals, sory neurons (5). Although TRPV1 et al. (2) could have some therapeutic where they project, and whether they plays a major role in heat hyperalgesia, utility. Linoleic acid metabolites have also receive input from other sensory deletion of TRPV1 or even the cells been associated with GPCR-mediated neurons. One caveat to these findings that express TRPV1 (6) has little effect signaling, as well as human pathologies results from the fact that TRPV1-null on heat sensing at threshold noxious ranging from type II diabetes to Alzhei- mutant mice can develop some mechan- temperatures (as opposed to very high mer’s disease (12, 13). ical hypersensitivity (5). There must, temperatures) measured with Har- therefore, be mechanisms that contrib- greaves’s eponymous apparatus. This Mechanisms of Allodynia observation suggests that other heat re- Although the expression of channels in ceptors in other cells have lower heat sensory neurons that contribute to Author contributions: U.O. and J.N.W. wrote the paper. thresholds than TRPV1 and signal nox- mechanosensation has been shown to be The authors declare no conflict of interest. ious heat independently (7). Is the prin- up-regulated both transcriptionally and See companion article on page 18820. cipal role of TRPV1 heat sensing? This in terms of membrane trafficking by in- 1To whom correspondence should be addressed. E-mail: possibility seems unlikely. The activation flammatory mediators, the development [email protected]. www.pnas.org͞cgi͞doi͞10.1073͞pnas.0910766106 PNAS ͉ November 3, 2009 ͉ vol. 106 ͉ no. 44 ͉ 18435–18436 ute to mechanosensitization that do not into how wiring dictates the actions of on other transient receptor potential ion require TRPV1. mediators. TRPV1 clearly has a number channels? Do these mediators cause of distinct functions, not all of which, TRPV1 activation directly or through Mediators, Receptors, Drugs, and Wiring particularly in the CNS, are understood. membrane effects? The recent paper (2) Will the enzymes that generate oxidized The role of linoleic acid metabolites as is likely to stimulate a wave of research linoleic acid products prove
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